Search PubMed⌕ Search

Biomedical subjects

D W Bell

Publications and source records attributed to D W Bell.

48 records · Page 3Linked to original sources
PubMed1993

The retinoblastoma-related gene, RB2, maps to human chromosome 16q12 and rat chromosome 19.

A retinoblastoma-related human gene, referred to as RB2, has been cloned based on sequence homology of the E1A-binding domain of the retinoblastoma gene. Structural homology with the retinoblastoma gene suggests a possible function of RB2 as a tumor suppressor gene. In this study, we have mapped this gene to human chromosome 16q12.2 and rat chromosome 19, using fluorescence in situ hybridization and somatic hybrid cell analysis, respectively. Based on known syntenic relationships among human, rat and mouse, the data suggest that the mouse homolog resides on chromosome 8. Deletions of chromosome 16q have been found in several human neoplasias (including breast, ovarian, hepatic, and prostatic cancers) which is in support of an involvement of RB2 in human cancer as a tumor suppressor gene.

Animals↗
PubMed1992

Early loss of heterozygosity on 17q in ovarian cancer. The Abe Ovarian Cancer Genetics Group.

We have studied 146 ovarian tumours (94 carcinomas, 22 tumours of low malignant potential and 30 benign tumours) for evidence of allele loss on chromosome 17p and 17q sufficient to imply the proximity of a tumour-suppressor gene. We have examined two polymorphic loci (YNZ22.2 and BHP53) on 17p13 and one on chromosome 17q (17q23-qter). Loss of heterozygosity (LOH) was detected in 34/63 (54%) informative malignant tumours at YNZ22.2 and 22/47 (47%) at BHP53; on 17q, 45/64 (70%) had LOH. Allele loss was detected in a small number of benign and borderline tumours. There was a statistically significant difference between the patterns of allele loss in serous and endometrioid groups of tumours, and allele loss occurred with significantly greater frequency on 17q than on 17p. Comparison of all malignant tumours presenting with either localized (FIGO stage I/II) or widespread (FIGO stage III/IV) disease showed that, particularly on 17q, allele loss increases in the more advanced stages. The p53 tumour-suppressor gene is implicated in ovarian carcinogenesis, and our findings suggest that an important tumour-suppressor gene may be located in the region 17q23-qter. Loss of function in this gene may be responsible for the frequently observed rapid progression of serous-type adenocarcinomas to an advanced stage.

Alleles↗
PubMed1981

Ulcerative colitis complicated by autoimmune hemolytic anemia.

We have reported the rare association of severe autoimmune hemolytic anemia with active ulcerative colitis, and added to the sparse published recommendations concerning management. Although aggressive medical therapy resulted in only partial control of the inflammatory bowel disease and hemolysis, both disorders remitted rapidly after panproctocolectomy and splenectomy. Autologous red cells were safely transfused during surgery.

Adult↗
PubMedDate not supplied

Laryngotracheoesophageal cleft: the anterior approach.

Laryngotracheoesophageal cleft was reported by Richter in 1792 after he examined an infant at autopsy and found a common lumen of esophagus and laryngotrachea. The next case was not noted until 1949 by Finlay. A recent review shows 40 cases in the world literature to date. Successful surgical approaches to some of these problems have basically employed a lateral pharyngotomy technique. In the case presented herein, the exact pathology was obscured by a severe tetralogy of Fallot and recurrent pneumonitis from a suspected high H-type tracheoesophageal fistula. The length of this cleft prompted an anterior approach with laryngo-fissure, cricoidotomy, and division of four tracheal rings for a complete and successful repair. Thorough endoscopy of all infants suspected of any laryngeal anomaly would yield an earlier diagnosis and opportunity for reconstruction of the cleft.

Diagnostic Errors↗